In several studies, prophylactic RT was found to be effective in preventing gynecomastia and mastodynia in patients with prostate cancer.2,11 However, although the high radiation doses may improve pain, they are less effective in reducing the volume of the tissue. In one study of the use of Tmx, 69% of prostate cancer patients in the high-dose bicalutamide (150 mg/day) group had gynecomastia, but this was reduced to only 9% in the group receiving both bicalutamide and Tmx (10-20 mg/day).30,31,32 Tmx must be continued throughout the anti-androgen therapy, since its effects do not persist after it has been discontinued. Anti-estrogens–In recent years, anti-estrogens have been increasingly used to decrease the stimulatory effects of estrogen on the male breast. Dehydrotestosterone (DHT) is a non-aromatizable androgen that has been approved for the treatment of gynecomastia in some countries and was found to be effective in uncontrolled studies.17,18 Danazole is a weak androgen that inhibits the secretion of LH and FSH from the pituitary. Gynecomastia caused by transient changes in hormone levels with growth usually disappears on its own within six months to two years. Gynecomastia is different from pseudogynecomastia or lipomastia, which refers to the presence of fat deposits in the breast area of obese men. While Gynaecomastia can appear in males of any age, there are several factors that make you more likely to have Gynaecomastia. Increased stress can stimulate the adrenal glands to secrete excess estrogen precursors. After dialysis, patients are free to resume a regular diet and often regain weight. Before dialysis, renal failure patients have restricted diets, can be malnourished and tend to lose weight. Gynecomastia is observed in approximately 50% of hemodialysis patients, primarily due to Leydig cell dysfunction. In addition, SHBG is often increased, leading to increased concentrations of E2. Primary hypogonadism can lead to decreased T production, compensatory LH increase, Leydig cell stimulation, the inhibition of 17, 20-lyase and 17-hydroxylase activities, elevated aromatization of T to E2 and finally an increase in the ratio of E2 to T. Patients who develop re-feeding gynecomastia are therefore often described to be undergoing a ‘second puberty’. In the lead re-feeding gonadotropins are increased, leading to T secretion and E2 production, which mimics normal puberty. It is recommended that physicians follow the algorithm for gynecomastia in patients under the age of 50 years, unless one of the atypical criteria shown in Figure 1 is met. In patients with pseudogynecomastia the fingers will not meet any resistance until they reach the nipple. In true cases of gynecomastia, the physician will feel a disc or firm tissue that is concentric with the nipple-areolar complex. Type 4 drugs act via unknown mechanisms and include isoniazid (INH), methyldopa, captopril, tricyclic antidepressants (TCAD), diazepam, heroin and cannabis.6,7 Spironolactone is a steroidal antimineralocorticoid and is one of the medications that have been most linked with gynecomastia. Gynecomastia can be typically classified into four grades of increasing severity, from I to IV, ranging from simple areolar protrusion, to breasts with a female appearance. It usually regresses within 18m and is uncommon in males aged 17 and older.8,11 The final peak occurs in older males (particularly in those aged years-old), with a prevalence of 24-65%. If differentiating between gynecomastia and breast cancer cannot be achieved using physical and imaging findings, a percutaneous biopsy should be taken. Heterogeneous inversion or polymorphism of the p450 aromatase gene leads to increased aromatase activity in peripheral tissues, resulting in elevated estrogen levels. Gynecomastia in patients with cirrhosis or liver disease is caused by increased production of androstenedione (A) from adrenal glands, increased aromatization of A to E1, increased conversion of E1 to E2, decreased clearance of adrenal androgens from the liver and increased SHBG, which leads to a decrease in free T levels. Medications have been reported to cause up to 25% of cases of gynecomastia and they can be categorized by their hormone-like action.6,10 Type 1 medications act like estrogens and include diethylstilbestrol (DEB), oral contraceptives, phytoestrogens, digitalis and estrogen-containing cosmetics. Gynecomastia develops when there is an imbalance between testosterone and estrogen, for example when testosterone activity is reduced or blocked, or when estrogen levels are relatively higher. The provider may also order blood tests to check estrogen and testosterone levels, as well as tests to assess kidney, liver, and thyroid function. Healthcare providers might recommend regular monitoring to track changes in breast tissue and overall health. In severe cases, the enlarged breast tissue can be painful or tender.
